DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on June 8, 2026, has been entered.
Response to Arguments
The Double Patenting Rejection is withdrawn as the examiner has reconsidered the distinction of the claimed subject population in the co-pending application.
Applicant’s arguments and previously set forth allegations of unexpected results have been fully considered and are responded to below in the context of the Examiner’s notes.
The examiner notes that a prima facie showing is established because PI3K inhibitors are taught to provide a reasonable expectation of success in treating PDAC pancreatic cancers. Conway concludes the following: The emerging efficacy of PI3K pathway inhibitors for PDAC and the convergence of several aberrantly expressed signaling cascades highlights a clear progression towards their application for this disease. For example, patients with aberrant DNA damage repair pathways have responded well to PI3K pathway inhibition as part of combination therapies, and trials are already underway in PDAC. Furthermore, given the complex dimerisation of the ErbB family of RTKs and the association of Ephrin receptors with more aggressive PDAC subtypes, RTKs may provide biomarkers for patients that would respond efficaciously to PI3K pathway inhibition. Table 2 provides a list of PI3K pathway inhibitors under clinical development for pancreatic cancers. Table 2 includes a vast number of agents. Conway also states: “Collectively, we see strong evidence accumulating for the efficacy of upstream isoform-specific targeting of PI3K in emerging PDAC combination therapies.” The use of a PIK3 inhibitors to treat pancreatic cancer is recognized as having a reasonable expectation of success.
While Conway provides a reasonable expectation of success that PI3K inhibitors, generally, will treat pancreatic cancer, Gaillard et al., (U.S. Pat. No. 9,073, 940) is an issued patent that claims compound 339 in prior art claim 6. Gaillard also explains that the compounds of Formula (I) are selective of the delta isoform of PI3K over the other isoforms. See col. 4, lines 56-57. “Furthermore, isoform-specific inhibition of PI3Kδ in cancer-associated immune cells was shown to downregulate their tolerance to PDAC, which improved the activity of T cells against the cancer.” See p745, last par. As such, Applicant’s characterization that Conway does not teach PI3Kδ inhibitors to treat pancreatic cancer, but only in relation to cancer generally appears to be a mischaracterization.
It further appears that the claimed compound, which has issued in a claimed is presumed valid at inhibiting PI3K and the prior art indicates that such compound preferentially inhibits isoform delta. Inhibiting isoform delta PI3K has been shown to be effective in treating PDAC cancer.
The examiner notes that patents are presumed valid and additionally data is not required to enable teachings of prior art.
The examiner notes that the claimed compound is known to work by inhibiting PI3Kδ isoform. And the inhibition of the PI3Kδ isoform is taught to improve T cell activity against PDAC cancer cells.
The fact that the claimed agent can treat other cancers does not prevent a prima facie showing from being established. There is a motivation to use each of the claimed agents taught by the cited prior art because they each work.
The examiner acknowledges that some picking and choosing was required to arrive at compound 339 taught by Gaillard. However, the examiner also notes that Gaillard teaches the claimed compound to work as a Table 1 compound to inhibit the PI3Kδ isoform. The compounds taught by Gaillard each have a reasonable expectation of success in doing so, thereby treating PDAC. Such mechanism of action is at least shown to improve a subject’s T cell response to PDAC cancer cells.
A prima facie showing is established and the examiner responded to Applicant’s allegations of unexpected results in the Final Office Action of March 30, 2026. There is no allegation or showing of unexpected results in Applicant’s Remarks of June 8, 2026.
Status of the Claims
Claims 1-12 are pending and examined.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1-12 are rejected under 35 U.S.C. 103 as being unpatentable over Wilkie et al., (US2016/0128311), in view of Tomasini et al., (US2020/0088732) (filed April 12, 2018), in view of Gaillard et al., (U.S. Pat. No. 9,073,940) (cited in IDS), in view of Conway et al., “Combating pancreatic cancer with PI3K pathway inhibitors in the era of personalized medicine,” JRW et al. Gut 2019;68:742-758, in view of Stockley et al., (U.S. Pat. No. 10,654,846).
Wilkie teaches methods for screening and treating pancreatic ductal adenocarcinoma (PDA) by administering taxanes, gemcitabine, and an Axl kinase inhibitor. See Abstract. Administration can be oral among many other acceptable routes of administration. See par. 11. The taxane that can be administered to treat PDA includes nab-paclitaxel in combination with gemcitabine for oral administration. See prior art claims 1, 11, 13, and 14. Pharmaceutically acceptable carriers and excipients can be used. Se par. 155. A preferred carrier for oral administration is a diluent. See par. 162. In some embodiments exemplary candidate drugs include inhibitors of PI3k, which can be administered with gemcitabine and/or paclitaxel. See par. 203.
Wilkie does not teach anti-PD-1 or anti-PD-L1 therapy.
Tomasini teaches treating PDA by administering gemcitabine and nab-paclitaxel. See par. 2. Additionally, treatment can also include inhibitors of PD-1, such as a PD-L1 ligand. See prior art claim 14. Administration can be oral or most other routes of administration. See par. 124, e.g.
Wilkie does not teach the claimed PI3K inhibitor (i.e., the compound of Formula (I)).
Gaillard teaches compounds that are PI3K inhibitors and they include compound 339 on page 69, which is shown below and is the claimed compound in claim 1.
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The compounds are PI3K inhibitors for treating conditions including cancer. See Abstract, p1 and prior art claim 8, e.g. Compositions can be administered orally. See p116, e.g. Gaillard explains that the compounds of Formula (I) are selective of the delta isoform of PI3K over the other isoforms. See col. 4, lines 56-57.
Gaillard does not teach PI3K inhibitors for treating PDAC.
Conway teaches PDAC accounts for about 95% of pancreatic cancers. A broad ranges of cancers are known to be a target for PI3K pathway, including pancreatic cancer. See p745, 1st par. Conway explains: “Collectively, this suggests that application of PI3K pathway inhibitors as a PDAC therapy may provide an opportunity for dual targeting of cancer cells and the deregulated cancer-associated stromal components.” Id. PDAC patients with high PI3K have a poorer survival rate than those with low activation of PI3K. See p745, 2nd par. Further, Conway explains: “Furthermore, isoform-specific inhibition of PI3Kδ in cancer-associated immune cells was shown to downregulate their tolerance to PDAC, which improved the activity of T cells against the cancer.” See p745, last par.
Stockley teaches the compound of claim 2 with a diluent or carrier in prior art claim 1, shown below.
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The compound above can be used to treat conditions including cancer as an autotaxin inhibitor. See Abstract. Stockley also teaches the cells that may be treated include those of proliferative disorders of the pancreas. As noted above by Conway, 95% of pancreatic cancers are PDAC. Thus, treating PDAC would be immediately envisaged in view of the teachings to treat pancreatic cancers, generally. Routes of administration for treatment include oral administration. See col. 48, line 2.
"It is prima facie obvious to combine two compositions each of which is taught by the prior art to be useful for the same purpose, in order to form a third composition to be used for the very same purpose.... [T]he idea of combining them flows logically from their having been individually taught in the prior art." In re Kerkhoven, 626 F.2d 846, 850, 205 USPQ 1069, 1072 (CCPA 1980).
It would have been prima facie obvious prior to the filing of the instant application to a person having ordinary skill in the art to arrive at the claimed methods in view of the cited prior art. One would be motivated to do so because: gemcitabine, nab-paclitaxel and anti-PD-1 therapies are known to be used to treat PDAC and pancreatic cancers when administered orally. Further, Gaillard teaches compounds that are PI3K inhibitors including the compound of claim 1 and Conway teaches that 95% of pancreatic cancers are PDAC and PI3K inhibitors are a therapeutic tool for treating the same. Thus, a POSA would have a reasonable expectation that the compound of claim 1 can treat cancers, pancreatic cancers, and PDAC. Moreover, Stockley teaches the compound recited in claim 2 as an autotaxin inhibitors that can treat proliferative disorders including pancreatic cancers. While Stockley does not teach PDAC explicitly, we know from Conway that 95% of pancreatic cancers are PDAC. Thus, it would not be reasonable to conclude with any statements to the contrary that an agent taught to treat pancreatic cancers would not be functional in treating 95% of pancreatic cancers that are PDAC. As such and in view of in re Kerkhoven, the use of gemcitabine, nab-paclitaxel, anti-PD-1 or anti-PD-L1 therapy, and administration of the claimed PI3K and autotaxin inhibitors would have a reasonable and predictable expectation of success in treating the claimed subject population based on their known and taught ability to treat the same subject population when administered orally with excipients as independent therapeutic agents.
As such, no claim is allowed.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JARED D BARSKY whose telephone number is (571)272-2795. The examiner can normally be reached on 9-5 M-F.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Amy Clark can be reached on 571-272-1310. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/JARED BARSKY/Primary Examiner, Art Unit 1628
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